Adverse effects of loop diuretics include:
Mild gastrointestinal disturbances, pancreatitis and hepatic encephalopathy
Hyperglycaemia
Acute urinary retention
Water and electrolyte imbalance
Hyponatraemia, hypocalcaemia, hypokalaemia, hypomagnesaemia, hypochloraemiaHypotension, hypovolaemia, dehydration, and venous thromboembolism
Metabolic alkalosis
Hyperuricaemia
Blood disorders (bone marrow suppression, thrombocytopenia, and leucopenia)
Visual disturbance, tinnitus and deafness
Hypersensitivity reactions

An acute focal or diffuse suppurative inflammation of the prostate gland is called acute bacterial prostatitis.

According to the National Institute for Health and Care Excellence (NICE), acute prostatitis should be suspected in a man presenting with:
A feverish illness of sudden onset which may be associated with rigors, arthralgia, or myalgia; Irritative urinary voiding symptoms; acute urinary retention; perineal or suprapubic pain and an exquisitely tender prostate on rectal examination.

Treatment of acute prostatitis as recommended by NICE and the BNFare:
Ciprofloxacin or ofloxacin for 14 days
Alternatively, trimethoprim can be used. Duration of treatment is still 14 days

The NICE guidelines for pregnant women with lower UTIs are:
1. Prescribe an antibiotic immediately, taking into account the previous urine culture and susceptibility results or avoiding past antibiotics that may have caused resistance
2. Obtain a midstream urine sample before starting antibiotics and send for urine culture and susceptibility
– Review the choice of antibiotic when the results are available
– change the antibiotic according to susceptibility results if the bacteria are resistant, using a narrow-spectrum antibiotic wherever possible

The first choice of antibiotics for pregnant women aged 12 years and over is:
1. Nitrofurantoin
100 mg modified-release PO BD for 3 days – if eGFR >45 ml/minute

The second-choice (no improvement in lower UTI symptoms on first-choice for at least 48 hours, or when first-choice is not suitable) are:
1. Amoxicillin
500 mg PO TDS for seven days (ONLY if culture results available and susceptible)
2. Cefalexin
500 mg BD for seven days
Alternative second-choices – consult local microbiologist, choose antibiotics based on culture and sensitivity results

Amlodipine is a calcium-channel blocker that is frequently used to treat hypertension. Ankle swelling is a very common side effect of calcium-channel blockers, and it occurs quite frequently.

Polydipsia is the feeling of extreme thirstiness. It is often linked to polyuria, which is a urinary condition that causes a person to urinate excessively. The cycle of these two processes makes the body feel a constant need to replace the fluids lost in urination. In healthy adults, a 3 liter urinary output per day is considered normal. A person with polyuria can urinate up to 15 liters of urine per day. Both of these conditions are classic signs of diabetes.

The other options are also types of diabetes, except for psychogenic polydipsia (PPD), which is the excessive volitional water intake seen in patients with severe mental illness or developmental disability. However, given the patient’s previous head injury, the most likely diagnosis is cranial diabetes insipidus.

By definition, cranial diabetes insipidus is caused by damage to the hypothalamus or pituitary gland after an infection, operation, brain tumor, or head injury. And the patient’s history confirms this diagnosis. To define the other choices, nephrogenic diabetes insipidus happens when the structures in the kidneys are damaged and results in an inability to properly respond to antidiuretic hormone.

Kidney damage can be caused by an inherited (genetic) disorder or a chronic kidney disorder. As with cranial diabetes insipidus, nephrogenic diabetes insipidus can also cause an elevated urine output.

Diabetes mellitus is classified into two types, and the main difference between them is that type 1 diabetes is a genetic disorder, and type 2 diabetes is diet-related and develops over time. Type 1 diabetes is also known as insulin-dependent diabetes, in which the pancreas produces little or no insulin. Type 2 diabetes is termed insulin resistance, as cells don’t respond customarily to insulin.

The first line treatment for acute gout includes NSAIDs like diclofenac, indomethacin or naproxen. In patients in whom NSAIDs are contraindicated, not tolerated or ineffective, colchicine is an alternative. In those who cannot tolerate or who are resistant to NSAIDs and colchicine, oral or parenteral corticosteroids are an effective alternative. In acute monoarticular gout, intra-articular injection of a corticosteroid can be used occasionally. In acute gout. allopurinol is not used in the actual treatment, but its use should be continued during an acute attack if the patient is already established on long term therapy.

Diabetes insipidus is the inability to produce concentrated urine. It is characterised by the presence of excessive thirst, polyuria and polydipsia. There are two distinct types of diabetes insipidus:
Cranial (central) diabetes insipidus and;
Nephrogenic diabetes insipidus
Cranial diabetes insipidus is caused by a deficiency of vasopressin (anti-diuretic hormone). Patients with cranial diabetes insipidus can have a urine output as high as 10-15 litres per 24 hours, but adequate fluid intake allows most patients to maintain normonatraemia. 30% of cases are idiopathic, and a further 30% are secondary to head injuries. Other causes include neurosurgery, brain tumours, meningitis, granulomatous disease (e.g. sarcoidosis) and drugs, such as naloxone and phenytoin. A very rare inherited form also exists that is associated with diabetes mellitus, optic atrophy, nerve deafness and bladder atonia.
Nephrogenic diabetes insipidus is caused by renal resistance to the action of vasopressin. As with cranial diabetes insipidus, urine output is markedly elevated. Serum sodium levels can be maintained by secondary polydipsia or can be elevated. Causes of nephrogenic diabetes insipidus include chronic renal disease, metabolic disorders (e.g. hypercalcaemia and hypokalaemia) and drugs, including long-term lithium usage and demeclocycline.
In view of the history of long-term lithium use, in this case, nephrogenic diabetes insipidus is the most likely diagnosis.

Pectoralis major is a thick, fan-shaped muscle situated in the chest. It makes up the bulk of the chest musculature in the male and lies underneath the breast in the female. It overlies the thinner pectoralis minor muscle.
Superficial muscles of the chest and arm showing pectoralis major (from Gray’s Anatomy)
Pectoralis major has two heads; the clavicular head and the sternocostal head. The clavicular head originates from the anterior border and medial half of the clavicle. The sternocostal head originates from the anterior surface of the sternum, the superior six costal cartilages and the aponeurosis of the external oblique muscle. It inserts into the lateral lip of the bicipital groove of the humerus.
Pectoralis major receives dual innervation from the medial pectoral nerve and the lateral pectoral nerve.
Its main actions are as follows:
Flexes humerus (clavicular head)
Extends humerus (sternocostal head)
Adducts and medially rotates the humerus
Draws scapula anteriorly and inferiorly

Fludrocortisone has the most potent mineralocorticosteroid activity, making it ideal for mineralocorticoid replacement in adrenal insufficiency.

Insulin has a number of effects on glucose metabolism, including:
Inhibition of glycogenolysis and gluconeogenesis
Increased glucose transport into fat and muscle
Increased glycolysis in fat and muscle
Stimulation of glycogen synthesis
By inhibiting gluconeogenesis, insulin maintains the availability of amino acids as substrates for protein synthesis. Thus, insulin supports protein synthesis through direct and indirect mechanisms.